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. 2017 Jul 5;68(1):1–17. doi: 10.1007/s12576-017-0556-6

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© The Author(s) 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 3 — Schematic presentation of the mechanism of the vascular intrinsic clock that generates the circadian rhythm of the activity of myosin light chain phosphatase (MLCP). The circadian oscillation of the expression of the clock gene RORα is translated to the rhythmic changes in the expression and activity of ROCK2, which in turn causes the oscillatory changes in the phosphorylation of MYPT1, a regulatory subunit of MLCP, at Thr853 (pT853) and the phosphorylation of MCL (MLC-P) induced by receptor agonist, thereby generating diurnal changes in the vascular contractility. The processes, which exhibited a circadian rhythm in [20], are indicated by clock images. MLCP is composed of three subunits: a catalytic subunit PP1, MYPT1 and another regulatory subunit M20. The activity of MLCP is negatively regulated by the phosphorylation of MYPT1 at either Thr696 (pT696) or T853 (pT853). Therefore, when the expression of ROCK2 and the phosphorylation of MYPT1 are high (solid line curve), the activity of MLCP is considered to be reciprocally low (dashed line curve). MLC 20-kDa myosin light chain, RORα retinoic acid receptor-related orphan receptor α (see also Figs. 1, 2)